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Regulatory analysis of the mouse Fgf3 gene: Control of embryonic expression patterns and dependence upon sonic hedgehog (Shh) signalling
Author(s) -
Powles Nicola,
Marshall Heather,
Economou Androulla,
Chiang Chin,
Murakami Akira,
Dickson Clive,
Krumlauf Robb,
Maconochie Mark
Publication year - 2004
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20028
Subject(s) - sonic hedgehog , biology , enhancer , hedgehog signaling pathway , microbiology and biotechnology , hindbrain , embryonic stem cell , hedgehog , reporter gene , transgene , dorsal root ganglion , gene expression , genetics , gene , embryo , signal transduction , neuroscience , spinal cord
Fgf3 displays a dynamic and complex expression pattern during mouse embryogenesis. To address the molecular mechanisms underlying Fgf3 expression, we used a transgenic approach to assay genomic regions from the mouse Fgf3 gene for regulatory activity. We identified an enhancer that mediates major components of embryonic expression, governing expression in the midbrain, hindbrain, surface ectoderm, dorsal roots and dorsal root ganglia (DRG), proximal sensory ganglia, and the developing central nervous system (CNS). Deletional analysis of the enhancer further delimited this regulatory activity to a 5.7‐kb fragment. We have also revealed sonic hedgehog (Shh) ‐dependent and Shh‐independent aspects of Fgf3 expression through breeding the Fgf3 reporter transgene into Shh mutants. In the absence of Shh signalling, Fgf3 reporter expression is lost in the ventral CNS, DRG, and superior cervical nerves, whereas activation of reporter expression in cranial ganglion cells is Shh independent. Moreover, detailed re‐examination of the Shh phenotype revealed that Shh signalling is required for the correct development/maturation of the DRG. Developmental Dynamics 230:44–56, 2004. © 2004 Wiley‐Liss, Inc.